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Bone marrow mesenchymal stem cells-derived exosomal microRNA-16-5p restrains epithelial-mesenchymal transition in breast cancer cells via EPHA1/NF-κB signaling axis
Institution:1. Department of Oncology, Shaanxi Provincial People''s Hospital, Xi''an 710068, Shaanxi, China;2. Fujian Key Laboratory of Aptamer Technology, Affiliated Dongfang Hospital of School of Medicine, Xiamen University, China;3. Department of Clinical Laboratory Medicine, Fuzhou General Clinical Medical School, Fuzhou 350108, Fujian, China;4. the 900th Hospital, Fujian Medical University, Fuzhou 350108, Fujian, China;5. Department of Pathology, Shaanxi Provincial People''s Hospital, Xi''an 710068, Shaanxi, China;6. Xi''an Medical University, Xi''an 710021, Shaanxi, China;7. Department of Dermatology, Shaanxi Provincial People''s Hospital, Xi''an 710068, Shaanxi, China;8. Department of Emergency, Shaanxi Provincial People''s Hospital, Xi''an 710068, Shaanxi, China;9. Center for Reproductive Medicine, Naval Medical Center, Second, Military Medical University, Shanghai 200052, China
Abstract:ObjectiveThis study intends to conquer the mystery of microRNA-16-5p/erythropoietin-producing hepatocellular A1/nuclear factor-κB signaling (miR-16-5p/EPHA1/NF-κB signaling) in breast cancer.MethodsExpression of miR-16-5p, EPHA1 and NF-κB signaling-related proteins were detected. Gene overexpression or silencing was used to examine the biological roles of bone marrow mesenchymal stem cells (BMSCs)-derived exo-miR-16-5p in breast cancer. The effect of exo-miR-16-5p on tumorigenesis of breast cancer was confirmed by the xenograft nude mouse model.ResultsLow miR-16-5p and high EPHA1 expression were examined in breast cancer. BMSCs-derived exosomes, up-regulated miR-16-5p or down-regulated EPHA1 restrained epithelial-mesenchymal transition (EMT) of breast cancer cells and tumor growth in nude mice. Down-regulated miR-16-5p or up-regulated EPHA1 activated NF-κB signaling. Knockdown of EPHA1 or inhibition of NF-κB signaling reversed the effects of down-regulated miR-16-5p on breast cancer cells.ConclusionBMSCs-derived exosomal miR-16-5p hinders breast cancer cells progression via EPHA1/NF-κB signaling axis.
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